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Abstract: Aims: Readmissions for heart failure (HF) are a major burden. We aimed to assess whether the extent of improvement in pulmonary fluid content (ΔPC) during HF hospitalization evaluated by lung impedance (LI), or indirectly by other clinical and laboratory parameters, predicts readmissions. Methods and results: The present study is based on pre‐defined secondary analysis of the IMPEDANCE‐HF extended trial comprising 266 HF patients at New York Heart Association Class II–IV and left ventricular ejection fraction ≤ 35% randomized to LI‐guided or conventional therapy during long‐term follow‐up. Lung impedance‐guided patients were followed for 58 ± 36 months and the control patients for 46 ± 34 months (P < 0.01) accounting for 253 and 478 HF hospitalizations, respectively (P < 0.01). Lung impedance, N‐terminal pro‐brain natriuretic peptide, weight, radiological score, New York Heart Association class, lung rales, leg oedema, or jugular venous pressure were measured at admission and discharge on each hospitalization in both groups with the difference defined as ΔPC. Average LI‐assessed ΔPC was 12.1% vs. 9.2%, and time to HF readmission was 659 vs. 306 days in the LI‐guided and control groups, respectively (P < 0.01). Lung impedance‐based ΔPC predicted 30 and 90 day HF readmission better than ΔPC assessed by the other variables (P < 0.01). The readmission rate for HF was lower if ΔPC > median compared with ΔPC ≤ median for all parameters evaluated in both study groups with the most pronounced difference predicted by LI (P < 0.01). Net reclassification improvement analysis showed that adding LI to the traditional clinical and laboratory parameters improved the predictive power significantly. Conclusions: The extent of ΔPC improvement, primarily the LI based, during HF‐hospitalization, and study group allocation strongly predicted readmission and event‐free survival time. [ABSTRACT FROM AUTHOR]

This case report describes a 37-year-old female who was admitted to our Emergency Department because of shortness of breath. On physical examination, she had dyspnea and tachycardia and blood pressure was 80/50 mmHg with a pulsus paradoxus of 22 mmHg. Neck veins were distended, heart sounds were distant, and dullness was found on both lung bases. Her chest X-ray revealed bilateral pleural effusion and cardiomegaly. On both computed tomography and echocardiography the heart was of normal size and a large pericardial effusion was noted. The echocardiogram showed signs of impending tamponade, so the patient underwent an emergent pericardiocentesis. No infectious etiology was found and she was assumed to have viral pericarditis and was treated accordingly. However, when the pericardial effusion recurred and empirical therapy for tuberculosis failed, a pericardial window was performed. A typical staining pattern for mesothelioma was found on her pericardial biopsy specimen. Since no other mesodermal tissue was affected, a diagnosis of primary malignant pericardial mesothelioma was made. Chemotherapy was not effective and she passed away a year after the diagnosis was made. This case highlights the difficulties in diagnosing this uncommon disease in patients that present with the common finding of pericardial effusion. [ABSTRACT FROM AUTHOR]

Leukaemia inhibitory factor (LIF) and interleukin (IL)-6 are members of a cytokine group that share a common signal transducer gp130 and induce pleiotropic biological effects in cells of diverse lineage. In monocytes, LIF facilitates differentiation, which may stimulate the biosynthesis of tissue factor (TF) that initiates the coagulation cascade. We tested the hypothesis that LIF would enhance TF expression in human monocyte-derived macrophages (MDMs). Human peripheral blood mononuclear cells separated from whole blood by density centrifugation were allowed to differentiate into MDMs in primary culture, and were then exposed to LIF, IL-6 and oncostatin M (OSM) for 24 h. LIF and IL-6 receptors, and gp130 were demonstrated in MDMs by immunocytochemistry and RT-PCR. TF procoagulant activity (TF-PCA) was measured by recalcification clotting time and TF protein by Western blotting. The results show that both TF procoagulant activity and TF protein increased significantly in response to LIF over the concentration range of 1–100 nm (P < 0.03). Although OSM and IL-6 tended to enhance TF expression by MDMs, the increase did not reach statistical significance. Anti-LIF receptor and anti-gp130 antibodies attenuated the effect of LIF on TF expression as assayed by both bioassay and flow-cytometry. In conclusion, LIF increases TF-PCA and TF protein in MDMs, and specific anti-LIF receptor antibodies attenuate this effect. Thus, LIF may regulate by a gp130-dependent pathway macrophage-mediated procoagulant function in diverse pathological states involving inflammation and thrombosis and seems to serve as an important mediator at the interface between these processes. [ABSTRACT FROM AUTHOR]